Abstract
Mutations in isocitrate dehydrogenase isoform (IDH) 1 and 2 occur in approximately 25% of patients with acute myeloid leukemia (AML). These mutations lead to a block in myeloid differentiation and ultimately, to the development of AML. Inhibitors of mutant IDH1 and 2 have recently been approved by the US Food and Drug Administration and their use has led to clinical responses with prolonged duration of response. IDH inhibitors in combination with standard-of-care therapy and other small molecular inhibitors are now being used.
Keywords:
Acute myeloid leukemia; Beta-hydroxyglutarate; Enasidenib; Isocitrate dehydrogenase; Ivosidenib.
Copyright © 2018 Elsevier Inc. All rights reserved.
MeSH terms
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Animals
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Antineoplastic Agents / pharmacology
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Antineoplastic Agents / therapeutic use
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Antineoplastic Combined Chemotherapy Protocols / adverse effects
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Antineoplastic Combined Chemotherapy Protocols / therapeutic use
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Biomarkers
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Enzyme Inhibitors / pharmacology
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Enzyme Inhibitors / therapeutic use
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Humans
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Isocitrate Dehydrogenase / genetics
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Isocitrate Dehydrogenase / metabolism*
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Isoenzymes
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Leukemia, Myeloid, Acute / diagnosis
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Leukemia, Myeloid, Acute / drug therapy*
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Leukemia, Myeloid, Acute / etiology
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Leukemia, Myeloid, Acute / metabolism*
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Molecular Targeted Therapy
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Mutation
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Protein Processing, Post-Translational
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Treatment Outcome
Substances
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Antineoplastic Agents
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Biomarkers
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Enzyme Inhibitors
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Isoenzymes
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Isocitrate Dehydrogenase